A review on inflammatory cytokine-induced alterations of the brain as potential neural biomarkers in post-traumatic stress disorder

Yong Ku Kim, Meysam Amidfar, Eunsoo Won

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The heterogeneity of post-traumatic stress disorder (PTSD) symptoms indicates that multiple neurobiological mechanisms underlie the pathophysiology of the condition. However, no generally accepted PTSD biomarkers in clinical practice currently exist. The sequential responses to recurrent and chronic stress by the hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous system (ANS) system are considered to play a significant role in the onset and progression of PTSD. Decreased activity of the HPA axis and parasympathetic nervous system, along with increased activity of the sympathetic nervous system, have been observed in PTSD, which may lead to increased levels of proinflammatory cytokines. Such heightened activity of the immune system may cause alterations in the structure and function of brain regions—for example, the amygdala, hippocampus, medial prefrontal cortex, anterior cingulate cortex, and insula—through changes in levels of serotonin and kynurenine pathway metabolites, and direct neurotoxic effects of cytokines. Although chronic inflammation-induced alterations in brain regions critical in controlling emotional behavior and fear regulation may represent a strong candidate biomarker of PTSD, future studies are necessary to further elucidate inflammation-associated neural biomarkers of PTSD. Continued research on therapeutic methods that involve the normalization of the HPA axis, ANS, and immune system is expected to contribute to the development of novel ways to treat PTSD.

Original languageEnglish
JournalProgress in Neuro-Psychopharmacology and Biological Psychiatry
DOIs
Publication statusAccepted/In press - 2018 Jan 1

Fingerprint

Post-Traumatic Stress Disorders
Biomarkers
Cytokines
Brain
Autonomic Nervous System
Immune System
Parasympathetic Nervous System
Therapeutic Human Experimentation
Inflammation
Kynurenine
Gyrus Cinguli
Sympathetic Nervous System
Amygdala
Prefrontal Cortex
Fear
Hippocampus
Serotonin

Keywords

  • Amygdala
  • Anterior cingulate cortex
  • Autonomic nervous system
  • Hippocampus
  • Hypothalamic–pituitary–adrenal axis
  • Insula
  • Medial prefrontal cortex
  • Posttraumatic stress disorder
  • Proinflammatory cytokines
  • Stress

ASJC Scopus subject areas

  • Pharmacology
  • Biological Psychiatry

Cite this

@article{13a0285e536a455db6fde0cd91d69912,
title = "A review on inflammatory cytokine-induced alterations of the brain as potential neural biomarkers in post-traumatic stress disorder",
abstract = "The heterogeneity of post-traumatic stress disorder (PTSD) symptoms indicates that multiple neurobiological mechanisms underlie the pathophysiology of the condition. However, no generally accepted PTSD biomarkers in clinical practice currently exist. The sequential responses to recurrent and chronic stress by the hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous system (ANS) system are considered to play a significant role in the onset and progression of PTSD. Decreased activity of the HPA axis and parasympathetic nervous system, along with increased activity of the sympathetic nervous system, have been observed in PTSD, which may lead to increased levels of proinflammatory cytokines. Such heightened activity of the immune system may cause alterations in the structure and function of brain regions—for example, the amygdala, hippocampus, medial prefrontal cortex, anterior cingulate cortex, and insula—through changes in levels of serotonin and kynurenine pathway metabolites, and direct neurotoxic effects of cytokines. Although chronic inflammation-induced alterations in brain regions critical in controlling emotional behavior and fear regulation may represent a strong candidate biomarker of PTSD, future studies are necessary to further elucidate inflammation-associated neural biomarkers of PTSD. Continued research on therapeutic methods that involve the normalization of the HPA axis, ANS, and immune system is expected to contribute to the development of novel ways to treat PTSD.",
keywords = "Amygdala, Anterior cingulate cortex, Autonomic nervous system, Hippocampus, Hypothalamic–pituitary–adrenal axis, Insula, Medial prefrontal cortex, Posttraumatic stress disorder, Proinflammatory cytokines, Stress",
author = "Kim, {Yong Ku} and Meysam Amidfar and Eunsoo Won",
year = "2018",
month = "1",
day = "1",
doi = "10.1016/j.pnpbp.2018.06.008",
language = "English",
journal = "Progress in Neuro-Psychopharmacology and Biological Psychiatry",
issn = "0278-5846",
publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - A review on inflammatory cytokine-induced alterations of the brain as potential neural biomarkers in post-traumatic stress disorder

AU - Kim, Yong Ku

AU - Amidfar, Meysam

AU - Won, Eunsoo

PY - 2018/1/1

Y1 - 2018/1/1

N2 - The heterogeneity of post-traumatic stress disorder (PTSD) symptoms indicates that multiple neurobiological mechanisms underlie the pathophysiology of the condition. However, no generally accepted PTSD biomarkers in clinical practice currently exist. The sequential responses to recurrent and chronic stress by the hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous system (ANS) system are considered to play a significant role in the onset and progression of PTSD. Decreased activity of the HPA axis and parasympathetic nervous system, along with increased activity of the sympathetic nervous system, have been observed in PTSD, which may lead to increased levels of proinflammatory cytokines. Such heightened activity of the immune system may cause alterations in the structure and function of brain regions—for example, the amygdala, hippocampus, medial prefrontal cortex, anterior cingulate cortex, and insula—through changes in levels of serotonin and kynurenine pathway metabolites, and direct neurotoxic effects of cytokines. Although chronic inflammation-induced alterations in brain regions critical in controlling emotional behavior and fear regulation may represent a strong candidate biomarker of PTSD, future studies are necessary to further elucidate inflammation-associated neural biomarkers of PTSD. Continued research on therapeutic methods that involve the normalization of the HPA axis, ANS, and immune system is expected to contribute to the development of novel ways to treat PTSD.

AB - The heterogeneity of post-traumatic stress disorder (PTSD) symptoms indicates that multiple neurobiological mechanisms underlie the pathophysiology of the condition. However, no generally accepted PTSD biomarkers in clinical practice currently exist. The sequential responses to recurrent and chronic stress by the hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous system (ANS) system are considered to play a significant role in the onset and progression of PTSD. Decreased activity of the HPA axis and parasympathetic nervous system, along with increased activity of the sympathetic nervous system, have been observed in PTSD, which may lead to increased levels of proinflammatory cytokines. Such heightened activity of the immune system may cause alterations in the structure and function of brain regions—for example, the amygdala, hippocampus, medial prefrontal cortex, anterior cingulate cortex, and insula—through changes in levels of serotonin and kynurenine pathway metabolites, and direct neurotoxic effects of cytokines. Although chronic inflammation-induced alterations in brain regions critical in controlling emotional behavior and fear regulation may represent a strong candidate biomarker of PTSD, future studies are necessary to further elucidate inflammation-associated neural biomarkers of PTSD. Continued research on therapeutic methods that involve the normalization of the HPA axis, ANS, and immune system is expected to contribute to the development of novel ways to treat PTSD.

KW - Amygdala

KW - Anterior cingulate cortex

KW - Autonomic nervous system

KW - Hippocampus

KW - Hypothalamic–pituitary–adrenal axis

KW - Insula

KW - Medial prefrontal cortex

KW - Posttraumatic stress disorder

KW - Proinflammatory cytokines

KW - Stress

UR - http://www.scopus.com/inward/record.url?scp=85048986341&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85048986341&partnerID=8YFLogxK

U2 - 10.1016/j.pnpbp.2018.06.008

DO - 10.1016/j.pnpbp.2018.06.008

M3 - Article

C2 - 29932946

AN - SCOPUS:85048986341

JO - Progress in Neuro-Psychopharmacology and Biological Psychiatry

JF - Progress in Neuro-Psychopharmacology and Biological Psychiatry

SN - 0278-5846

ER -